Examples of inflammatory mediator in the following topics:
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- An inflammatory response can be caused by any of numerous inflammatory mediators released from innate immune system cells.
- After an inflammatory mediator is released in the bloodstream, a period of transient vasoconstriction, lasting only a few seconds, occurs.
- Then blood vessels expand to undergo vasodilation from the stimulus of the vasoactive inflammatory mediator, which increases blood flow to the area.
- Other inflammatory mediators, such as TNF-alpha and IL-1, increase the expression of adhesion molecules on vascular endothelial cells.
- When acute inflammation ends (typically by release of anti-inflammatory mediators such as IL-10 or an end to the release of inflammatory mediators) resolution will occur if the problem is alleviated.
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- Some of the more important ones include inflammatory mediators such as IL-1, IL-4, and IL-6, the potent anti-inflammatory IL-10, and other interleukins involved with T and B cell signaling following antigen presentation.
- One common interferon is IFN-gamma, a pyrogen involved in inflammatory response and macrophage and NK cell activation.
- By definition, inflammatory mediators in other classes of cytokines are also considered chemokines.
- This long-lasting inflammatory mediator and pyrogen can cause fever and inflammation for up to 24 hours.
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- It results from the release of inflammatory mediators and cytokines from mast cells and basophils.
- The mast cells and basophils react by releasing inflammatory mediators such as histamine.
- These mediators increase the contraction of bronchial smooth muscles, cause blood vessels to widen (vasodilation), increase the leakage of fluid from blood vessels, and depress the actions of the heart muscle.
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- It is characterized by inflammation of the lung parenchyma leading to impaired gas exchange with concomitant systemic release of inflammatory mediators causing inflammation, hypoxemia, and frequently resulting in multiple organ failure.
- If the underlying disease or injurious factor is not removed, the amount of inflammatory mediators released by the lungs in ARDS may result in a systemic inflammatory response syndrome (or sepsis if there is lung infection).
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- For example, the rhinovirus is typically acquired by direct contact; it binds to human ICAM-1 receptors through unknown mechanisms to trigger the release of inflammatory mediators.
- These inflammatory mediators then produce the symptoms.
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- Fever is an elevation of body temperature above the regulatory set point, mediated through the release of prostaglandin E2.
- PGE2 release comes from the arachidonic acid pathway, which also
produces inflammatory mediators such as thromboxane and leukotriene.
- This pathway is mediated by the enzymes
phospholipase A2 (PLA2), cyclooxygenase-2 (COX-2), and prostaglandin E2
synthase.
- These enzymes ultimately mediate the synthesis and release of
PGE2.
- For example, septic shock is a severe bacterial infection in which bacterial toxins stimulate pyrogen and inflammatory mediator activity causes high fever.
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- The adaptive immune response is mediated by B and T cells and creates immunity memory.
- There are two subdivisions of the adaptive immune system: cell-mediated immunity and humoral immunity.
- Cell mediated immunity is controlled by type 1 helper T cells (Th1) and cytotoxic T cells.
- This binding will cause degranulation and release of inflammatory mediators that start an immune response against the antigen.
- This process is the reason why memory B cells can cause hypersensitivity (allergy) formation, as circulating IgE from those memory cells will activate a rapid inflammatory and immune response.
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- One subclass of cytokines is the interleukin (IL), which mediates interactions between leukocytes (white blood cells).
- A mast cell is a leukocyte that produces inflammatory molecules, such as histamine, in response to large pathogens.
- A basophil is a leukocyte that, like a neutrophil, releases chemicals to stimulate the inflammatory response .
- Eosinophils and basophils produce additional inflammatory mediators to recruit more leukocytes.
- Neutrophils, dendritic cells, and macrophages release chemicals to stimulate the inflammatory response.
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- Upon initial exposure to a potential allergen, an allergic individual synthesizes antibodies of the IgE class; this class of antibodies also mediates the immune response to parasitic worms.
- These chemical mediators then recruit eosinophils which mediate allergic responses .
- Delayed hypersensitivity is a cell-mediated immune response that takes approximately one to two days after secondary exposure for a maximal reaction to be observed.
- This type of hypersensitivity involves the TH1 cytokine-mediated inflammatory response.
- Insulin-dependent (Type 1) diabetes mellitus arises from a destructive inflammatory TH1 response against insulin-producing cells of the pancreas.
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- They may also cause granule dependent cell-mediated apoptosis through the release of perforins, granzymes, and proteases.
- Neutrophils defend against bacterial or fungal infection and other very small inflammatory processes.
- They are also the predominant inflammatory cells in allergic reactions.
- Mast cells function similarly to basophils in that they often mediate inflammation, but are more common and arise from a different hemopoeitic lineage.
- T-lymphocytes participate in the cell-mediated immune response.